Biochemistry Department, Faculty of Veterinary Medicine, Van Yuzuncu Yil University, 65090, Van, Turkey.
Özalp Regional High School, Van Yuzuncu Yil University, 65090, Van, Turkey.
Biol Trace Elem Res. 2021 Oct;199(10):3700-3706. doi: 10.1007/s12011-020-02491-3. Epub 2020 Nov 16.
Prolonged exposure to high doses of fluoride causes chronic poisoning called fluorosis, which affects many tissues and causes serious health problems. This study was planned to investigate the apoptotic, autophagic, and necrotic molecular pathways of fluoride. Sodium fluoride (NaF) was administered to normal rat kidney epithelial (NRK-52E) cells. The NaF IC value was determined using the MTT assay. The expression of the genes in the autophagic, apoptotic, and necrotic pathways was determined by real-time PCR. It was determined that there were significant changes in NaF-induced molecular pathways depending on the time. There were no increases in apoptotic and necrotic pathway markers except for Atg3, an autophagy gene, at the 3rd and the 12th hours. However, there was an induction in all cell death signaling pathways at 24 h. The molecular mechanisms demonstrated NaF-induced cellular death in the NRK-52E cell line. It was concluded that these molecular mechanisms were activated with NaF, and different mechanisms accelerated the cellular death at the 24th hour.
长期暴露于高剂量的氟化物会导致慢性中毒，称为氟中毒，它会影响许多组织并导致严重的健康问题。本研究旨在探讨氟化物的凋亡、自噬和坏死分子途径。向正常大鼠肾上皮（NRK-52E）细胞中添加氟化钠（NaF）。通过 MTT 测定法确定 NaF 的 IC 值。通过实时 PCR 确定自噬、凋亡和坏死途径中的基因表达。结果表明，随着时间的推移，NaF 诱导的分子途径发生了显著变化。除自噬基因 Atg3 外，在第 3 小时和第 12 小时，凋亡和坏死途径的标志物均未增加。然而，在 24 小时时，所有细胞死亡信号通路均被诱导。分子机制表明 NaF 诱导了 NRK-52E 细胞系中的细胞死亡。得出的结论是，这些分子机制被 NaF 激活，并且不同的机制在 24 小时加速了细胞死亡。
